Blood Pressure, Cerebral Blood Flow, and Outcome in Stroke The impact of a lower admission blood pressure (BP) on outcome in acute ischemic stroke is well documented. In the International Stroke Trial (1ST), every lOmmHg decrease in systolic blood pressure (SBP) under 150mmHg was associated with a 17.9% increase in the risk of early (2-week) death (International Stroke Trial Collaborative Group 1997, Leonardi-Bee 2002). Other studies have found similar results (Castillo 2004, Vemmos 2004, Okumura 2005, Yong 2005). There are theoretical reasons why a decrease in blood pressure can worsen injury in acute ischemic stroke. Astrup described the "ischemic penumbra," an area of at-risk brain surrounding a core of infarcted tissue that is electrically silent on electroencephalography but has intact ion pump function, and speculated that increasing perfusion to this area might lead to smaller eventual infarct size (Astrup 1981). In areas of acute ischemia, cerebral autoregulation is lost, and cerebral blood flow (CBF) is passively dependent on mean arterial pressure (MAP) (Eames 2002). A decreased MAP and decreased perfusion to this area might recruit more of the penumbra into the core of the stroke and worsen outcome. This leads to the question of whether increasing MAP will do the opposite. Patients with ischemic stroke have been shown to have areas of noninfarcted tissue with low, pressure-dependent, passive CBF that can be augmented by increasing blood pressure (Olsen 1983). Animal studies of focal ischemia have shown that induced hypertension increases intraluminal hydrostatic pressure, opens up collaterals, increases perfusion to the penumbra, and reduces ischemic injury (Cole 1990). Pressor therapy trials utilizing agents such as epinephrine, phenylephrine, and dopamine to raise systolic blood pressures (SBPs) to around 200mmHg (induced hypertension) have revealed that it improves both acute and chronic neurological deficits and increases rates of survival (Meier